© 2005 American Thoracic Society
Two-Year Cognitive, Emotional, and Quality-of-Life Outcomes in Acute Respiratory Distress SyndromeFrom the Authors:
Dr. Aberegg suggests that our study was limited by the use of surrogates to assess premorbid neurocognitive function. Premorbid neurocognitive disability in our patients was identified by chart review, interview of the significant other, and patient interview prior to signing informed consent (1). Our ARDS patients are younger (mean age 46 ± 16 years) than typically associated with age-related cognitive impairment or dementia (mean age We thank Dr. Aberegg for his suggestion that smoking and alcohol abuse may be risk factors for neurocognitive and affective sequelae. We compared the prevalence of neurocognitive sequelae using Fisher's exact tests, and depression and anxiety scores using independent t tests. All reported p values are two-sided. There was no difference in the prevalence of neurocognitive sequelae for smokers (n = 29) compared with nonsmokers (n = 38) at 1 year (p = 0.45) or 2 years (p = 0.14). There was no difference in the prevalence of neurocognitive sequelae for patients with a history of alcohol abuse (n = 13) compared with nonabusers (n = 54) at 1 year (p = 0.36) or 2 years (p = 0.53). Smokers had higher Beck Depression Inventory Scores (BDI) at 1 year (p = 0.05) but not at 2 years (p = 0.09) compared with nonsmokers. There was no difference in Beck Anxiety Inventory Scores (BAI) for smokers compared with nonsmokers at 1 year (p = 0.09), but there was a significant difference at 2 years (p = 0.01). Patients with a history of alcohol abuse had higher BDI scores at 1 year (p = 0.006) and 2 years than nonabusers (p = 0.009). Patients with a history of alcohol abuse had higher BAI scores at 1 year (p = 0.03) and 2 years than nonabusers (p = 0.01). Thus, smoking and alcohol abuse were related to depression and anxiety but not to neurocognitive sequelae in our ARDS patients. We reiterate that mechanisms of brain injury are likely multifactorial (3). The mechanisms of the neurocognitive sequelae may be due to ARDS and/or to critical illness and its treatment. Possible mechanisms include hypoxia, hypotension (3), sedatives (4), delirium (5), and hyperglycemia (6). The degree of neurocognitive impairment does not appear to be related to age, or the characteristics or severity of the critical illness (3).
a LDS Hospital, Salt Lake City, Utah, and Brigham Young University, Provo, Utah FOOTNOTES Conflict of Interest Statement: R.O.H. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript; L.K.W. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript; K.J.C. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript; J.F.O. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. REFERENCES
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